The NOX (NADPH oxidase) homolog, dual oxidase 1 (DUOX1), is expressed in the airway epithelium, and contributes to epithelial responses for various environmental triggers, such as allergens, by an oxidant-dependent cell signaling mechanism. DUOX1 is important in the allergen-induced epithelial production of the cytokine IL-33, which is a strong determinant of allergic asthma. DUOX1 may be enhanced in subjects with allergic asthma. DUOX1 may also contribute to several features of allergic asthma, such as TH2 cytokine production, mucus metaplasia, airway remodeling with subepithelial collagen deposition, and airway hyperresponsiveness, based on mice models. However, although antioxidant-based approaches have been successful in inhibiting allergic asthma in animal models, such approaches have not translated well to human asthma. Pharmacological approaches to target NOX enzymes have primarily targeted NADPH oxidase activation mechanisms that are not applicable to DUOX1, and so far none have been tested towards DUOX1. Accordingly, the inhibition of DUOX1 has not been well studied.